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Regulation and function of Arabidopsis UMAMIT amino acid transport facilitators in response to dark-induced energy starvation

Subject Area Plant Genetics and Genomics
Term from 2019 to 2024
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 426670491
 
Final Report Year 2024

Final Report Abstract

Plants possess an enormous plasticity to adapt their metabolism to the fluctuating energy supply in a natural environment. Recently, we defined the Arabidopsis Snf1 RELATED PRO- TEIN KINASE1 (SnRK1) and the down-stream network of C/S1 bZIP (BASIC LEUCINE ZIP- PER) transcription factors as a crucial module which controls catabolic processes to sustain plant’s energy homeostasis. Applying phenotypical, transcriptomic and ChIPseq approaches, a collection of group S1 bZIP mutants was studied to dissect their function in starvation response. Using DIS (Dark Induced Senescence) as an experimental system, we excluded bZIP2, bZIP11 and bZIP44 to function in starvation response. In contrast, the redundantly acting bZIP1 and bZIP53 control a co-expression network governing aa (amino acid) catabolism and transport, gluconeogenesis and energy homeostasis. Moreover, they regulate genes involved in asparagine – glutamine balance, critical for C/N homeostasis. This transcriptional reprogramming was found to be required for survival during starvation and regaining meristematic activity during recovery from stress. Thus, we provide insights in the transcriptional control of resource and energy management during starvation. As a second topic, we identified AtAVT6D and UMAMIT33 (USUALLY MULTIPLE AMINO ACIDS MOVE IN AND OUT TRANSPORTER33), which perform as aa facilitators in plants. We confirmed that both genes are transcriptionally highly induced during DIS and are controlled by the SnRK1-bZIP1/bZIP53 module. UMAMIT33 was found to be localized in the tonoplast, suggesting a function in cellular aa distribution. Indeed, after DIS induced protein degradation/autophagy, transporters are required to deliver aa from the vacuole to the cytosol. Hence, loss-of-function and misexpression approaches have been used for UMAMIT33, as well as umamit multiple mutants and umamit33/atavt6d double konock-outs. Unfortunately, no phenotypical alterations in DIS response or cellular aa distribution were observed, which would further support their impact in DIS. Functional redundancy would be a likely explanation. To this end, further studies during DIS and on resource allocation during seedling establishment are ongoing.

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